Location: Toxicology and Mycotoxin Research
Title: The conserved global regulator veA is necessary for symptom production and mycotoxin synthesis in maize seedlings by Fusarium verticillioides Authors
|Myung, K -|
|Duvall, M -|
|Calvo, Ana -|
Submitted to: Plant Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 25, 2011
Publication Date: July 1, 2011
Repository URL: http://naldc.nal.usda.gov/download/55007/PDF
Citation: Myung, K., Zitomer, N.C., Duvall, M., Glenn, A.E., Riley, R.T., Calvo, A.M. 2011. The conserved global regulator veA is necessary for symptom production and mycotoxin synthesis in maize seedlings by Fusarium verticillioides. Plant Pathology. (2012) 61:152-160. DOI: 10.1111/j.1365-3059.2011.02504.x. Interpretive Summary: A gene known as veA was previously identified in a group of plant pathogenic and toxin-producing fungi. The gene is necessary for biosynthesis of mycotoxins and other secondary metabolites in these fungi. This current study includes a survey for veA in other fungi using bioinformatics and available genomic sequences. The presence of similar genes was noted for many other fungi, including species of Fusarium that are noted plant pathogens and toxin-producers. The veA gene was inactivated in Fusarium verticillioides, and these mutants were used to study the role of veA in infection and disease development on maize seedlings. The results from infection studies and toxin profiling reveal that veA is required for normal pathogenesis and toxin production by this fungus.
Technical Abstract: The veA or velvet gene is necessary for biosynthesis of mycotoxins and other secondary metabolites in Aspergillus species. In addition, veA has also been demonstrated to be necessary for normal seed colonization in Aspergillus flavus and Aspergillus parasiticus. The present study shows that veA homologs are broadly distributed in fungi, particularly in Ascomycetes. The Fusarium verticillioides veA ortholog, FvVE1, is also required for the synthesis of several secondary metabolites, including fumonisin and fusarins. We also show that maize plants grown from seeds inoculated with FvVE1 deletion mutants did not show disease symptoms, while plants grown from seeds inoculated with the F. verticillioides wild-type and complementation strains clearly showed disease symptoms under the same experimental conditions. In this latter case, the presence of lesions coincided with accumulation of fumonisins in the plant tissues, and only these plant tissues had elevated levels of sphingoid bases and their 1-phosphate derivatives, indicating inhibition of ceramide synthase and disruption of sphingolipid metabolism. Our results strongly suggest that FvVE1 is necessary for pathogenicity by F. verticillioides against maize seedlings. The conservation of veA homologs among ascomycetes suggests that veA could play a pivotal role in regulating secondary metabolism and associated pathogenicity in other fungi.